Central Mechanism of Pain (7/10/15) Flashcards
What area of the Brainstem is associated with pain?
The Caudalis (Medullary dorsal horn) which is the Inferior portion of Medulla. *This is also part of the spinal trigeminal nucleus
What Types of neurons do you find in the Medullary Dorsal Horn?
You have: Nociceptive Specific Neurons - painful mechanical stimuli Wide Range Dynamic Neurons - Light touch - Painful mechanical stimuli - Noxious Heat
*Note: the Nociceptors are usually more restricted to superfical layer of the MDH.
Nociceptive specific neurons terminate mostly in ____________ layers of the MDH.
Superficial layers I and II
Non-nociceptive neurons terminate mostly in _________ layers of the MDH.
Deeper layers III, IV and V
*There is overlap in layers II and V
Describe Convergence in the MDH. What does it mean? and What happens?
Convergence refers to the phenomenon of multiple sensory receptors giving information to a smaller number of neural cells.
In the MDH Convergence leads to the emergence of wide dynamic range neurons.
What does the Convergence of peripheral afferent with different receptive fields cause?
Well, when you have convergence of cutaneous, joint, muscle and other nerves it can be a substrate for referred pain.
*MDH can be substrate for referred pain.
Is Referred pain a normal condition? What (several) factors contribute to it.
No! It only occurs under pathological conditions.
These factors can contribute to it:
- Convergence in MDH (Pain and non-pain) afferents converging on “pain-signaling” neuron.
- Peripheral sensitization that occurs with inflammation 7 nerve damage (However, this mostly increases c-fiber sensitivity so it cannot be solely responsible)
What is Allodynia?
Feeling pain from a stimuli that should not be painful. *One of the 2 characteristics of central sensitization.
What is Hyperalgesia?
Feel EXCESSIVE pain from a stimuli that shouldn’t have been that painful. *The second of the 2 characteristics of central sensitization
What is Central sensitization?
Basically, when a stimuli can be either magnified or misconstrued (neurally) to be painful or sometimes both.
What evidence do we have that supports Central sensitization?
If you inject capsaicin into a hand, pain will be felt at the injection and all around it.
However, if you block the A-delta and A-beta fibers pain is no localized to only where the capsaicin actually is! (Due to C-fibers)
Describe the Process of Central sensitization…..
First, it begins with a barrage on C-fibers (acute pain or inflammation) this will lead to…
MDH Neuron Responses
- depolarization by substrate P (Tachykinin)
- Modification of NMDA receptors (Removal of Mg++ block)
- Increase in Conductance of NMDA receptor
Which will cause…….
Previously ineffective A-fibers to become effective!
- A-fibers release of glutamate effective at NMDA receptor now = larger receptive field.
- Response to innocuous stimuli induces pain (A-beta fibers)
Describe Central sensitization following Pulpitis…..
So you have inflamed teeth on one side of your mouth and yet you still have a lower pain threshold in contralateral healthy teeth. Why? B/C the inflamed teeth are “sensitizing” central neurons with input to make Healthy teeth more sensitive!
*This is due to central sensitization and Convergence.
Is pain confined to the MDH?
No..Trigeminal and pons can play a part too!
What is a Trigeminal Tractotomy?
Cutting select fiber to the MDH to prevent pain.
What are the effects of a trigeminal Tractotomy?
If C1-C3 (all afferents) are cut you can expect the following:
- Loss of thermal and light touch to the back of the head.
- Normal thermal and touch to face, but no pain.
- Hypolgesia in intraoral region
- Pupal pain remains intact!
What are the effects of a central lesion in the pons?
Diminishes intramural and premolar pain along with intraoral touch and thermal.
There are multiple pain pathways, what are the 3 you need to know?
- Afferents -> MDH -> N. Submedius -> cingulate cortex = emotional experience of pain
- Afferents -> MDH -> VPL (Thalamus) -> S1 (cortex) = sensory aspect of pain
- Afferents -> MDH -> Pons and Medulla (RF and oral motor Nerve (jaw-opening reflex, increased HR and BP))
What is the response to pain/stimuli in the VPM (Not VPL!)?
- Small receptive field so it’s good at locating “Where” the stimulus is applied.
- It tracks the onset/offset of the stimulus so it knows “when” it is applied.
- The stimulus creates a linear response here.
What is the repose to pain/stimuli in N. Submedius?
- Larger receptive field so it’s NOT good at locating stimulus precisely.
- The response outlasts the stimulus
- Neural representation of negative emotion outlasts the stimulus.
How does Phantom Pain occur?
Phantom pain is due to peripheral changes such as:
- sprouting
- Ectopic impulses
- Ephaptic transmission
- Up/down regulation of neurotransmitters, channels and transduction molecules
AND Central changes such as:
- Sprouting
- central sensitization (unmasking of synapses)
The N. Submedius and Cingulate cortex do what?
Process the emotional component of pain
*Neural response outlasts the stimulus (Poor localization)
The VPL and somatosensory cortex do what?
- Localization of pain (small receptive field)
- Tracks pain stimulus onset and offset
- May mediate phantom pain through reorganization
How can forebrain bundles modulate pain perception?
- Anxiety can increase pain perception.
- Placebo effect can suppress pain perception.
T or F, Anterior cingulate cortex is susceptible to opioids.
True!
Describe the Descending control of Pain…
Multiple CNS sites modulate pain:
- Forebrain ant. cingulate cortex = anxiety and placebo effect
- Midbrain Periaquaductal grey = pain suppression
- Rostral ventromedial medulla
* Many of these sites contain Endogenous opioids to suppress pain!
